An original speculative concept is proposed stressing the role of lipid peroxidation (l.p.) as primary injury in the process of the development of arteriosclerotic lesion. Lipid peroxidation distraction involves not only unsaturated fatty acid, constituents of cell biomebranes, but is an integral part of platelet aggregation. Due to l.p. damage to biomembranes, a labilization of lysosomes with release of enzymes follows with a denudation of basement membrane collagen. This prompts platelet aggregation with a new l.p. explosion, release of activators and mediators of nonspecific inflammatory injury. This process and development of tissue hypoxia in arterial wall is further stimulus for increased fibroblast activity, establishing a vicious circle. Another original part of this concept is that zinc is an integral part of various biomembranes where it contributes to the stabilization of these structures. One of the effects of zinc is related to inhibition of various forms of lipid peroxidation. Lipid peroxidation, being a metal-catalyzed reaction is inhibited by several chelating agents in vitro as well as in vivo. Some of these chelating agents (1,10-phenanthroline, 2,2'-dipyridyl) interfere also with collagen metabolism. Thus, effect of chelating agents on l.p. and collagen will be explored. A multidisciplinary approach includng biochemical, biological, and ultrastructural methods will be employed in rabbit and chicken models of arteriosclerosis studying various arteriosclerosis modifying agents.